Metabotropic glutamate receptor 5 (mGluR5) is abundant in neonatal astrocytes but decreases with ages, and is almost absent in the healthy adult brain. Astrocytic mGluR5 is important in formation of excitatory synapses. We previously showed that A2b receptor (A2BR), being upregulated in astrocytes, is responsible for down-regulation of Grm5 encoding mGluR5 during postnatal early development. Here, using A2BR knock out mice (A2BKO), we investigated effects of this loss of inhibitory control over mGluR5 during early development on adult brain functions. We firstly examined Grm5 expression level in the healthy adult (7 months old) cortical astrocytes. The Grm5 expression was twice as high in A2BKO mice as that of control wild-type mice (WT). Then, we performed two behavioral tests on A2BKO mice (9 to 11 weeks old). In von Frey test on naïve A2BKO mice, the percentage of maximum pain score of A2B mice was significantly higher than that of the WT mice. In temperature nociceptive threshold test, A2BKO mice exhibited lower threshold than WT mice. These results indicated that A2BKO mice are more sensitive to these sensory stimuli than WT mice, suggesting that astrocytic A2BR would contribute to form an appropriate sensory network in the cortex presumably via suppression of mGluR5-mediated synaptic remodeling.